This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The overarching goal of our studies is to develop a comprehensive structural and functional understanding of rod spherule and cone pedicle ribbon synaptic terminals. Vertebrate photoreceptors are nonspiking neurons that maintain sustained depolarization and neurotransmitter release from ribbon synapses in darkness and produce light-dependent graded hyperpolarizing responses. Photoreceptor apoptosis and visual deficits occur with inherited and toxicant-induced retinal degenerations, diseases, and aging. One such toxicant is lead. Blood lead concentrations equal to or less than the accepted 'safe level'of 10 microgram/dL result in retinal cognitive and visual-motor deficits. Postnatal only lead exposure produces rod-selective apoptosis and a subnormal scotopic electroretinogram (ERG) in mice and rats. Mitochondria in rod inner segments are primary sites of action. The cone inner segment mitochondria are not affected by postnatal lead exposure. However, the mitochondria in the presynaptic terminals of retinal photoreceptors--rod spherules and cone pedicles--have not yet been examined after lead exposure. To determine whether Bcl-xL overexpression, an anti-apoptotic protein, mitigates the long-term effects of postnatal lead exposure on pedicle and spherule mitochondria, we used transgenic mice overexpressing Bcl-xL in photoreceptors.